Rebound insomnia, a sleep disturbance characterized by a worsening of sleep beyond baseline levels following discontinuation of short-acting benzodiazepine hypnotics, has been identified. It has been hypothesized that this rebound leads to further use of hypnotics and ultimately to chronic hypnotic use or even misuse. Using all-night sleep recordings, as well as daytime and nighttime tests of sleep tendency, pharmacological determinants (dose effects and duration of drug use) of rebound insomnia will be studied. In addition, two hypotheses regarding the mechanisms of rebound will be evaluated. First, the degree to which sleep extension, while taking medication, leads to decreased sleep tendency on drug discontinuation will be studied. Finally, the relation of rebound and overmedication will be investagated by determining its relation to other known indicators of oversedation including anterograde amnesia and reduced arousability from sleep. There is a pressing need to collect objective and systematic information about rebound insomnia. The recently introduced shorter acting hypnotics (eg. temazepam, triazolam) are becoming more popular due to an absence of daytime residual effects following their nighttime use. And some hypnotics being developed are even shorter acting drugs. These shorter acting drugs are thought to have the greatest risk for rebound. Additionally, the recent consensus conference on drugs and insomnia organized by the National Institutes of Health recommended the use of shorter acting drugs as short-term symptomatic treatment of transient insomnias. Thus, an increasing number of otherwise healthy normal persons may be using these drugs to treat their transient insomnias, starting and stopping treatment many times (i.e. treating jet lag). However, rebound insomnia associated with these drugs may present a hazard making the appropriateness and safety of these trends in hypnotic prescribing and use questionable.